The objective of this study is to investigate the mechanism and role of cortisol effects on membrane function as reflected by changes in nucleoside transport and RNA synthesis, and their role in glucocorticoid-induced regression of lymphoma P1798. Cortisol induction or repression of specific classes of RNA essential for inhibition or maintenance of nucleoside transport will be investigated. Comparison of cortisol action in steroid-sensitive and steroid-resistant strains of p1798 will establish relevance of effects to tumor regression. BIBLIOGRAPHIC REFERENCES: Cortisol-Induced Lymphocytolysis of p1798 Tumor Cells in Glucose-free Pyruvate-free Medium. John Stevens and Yee Wan Stevens, J. Natl. Cancer Inst. 54, 1493-1494, 1975. Sequential Irreversible, Actinomycin D-sensitive, and Cycloheximide-sensitive Steps prior to Cortisol Inhibition of Uridine Utilization by p1798 Tumor Lymphocytes. John Stevens and Yee-Wan Stevens, Cancer Research 35, 2145-2153, 1975.